• Title/Summary/Keyword: cancer cell lines

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Expression of Survivin and HIAP-1 in Korean Gastric Cancers (한국인 위암에서 Survivin과 HIAP-1 유전자 발현)

  • Park Chan Jin;Ryu Seung Wan;Kim In Hoo;Baek Won-Ki;Suh Seong-Il;Suh Min-Ho;Sohn Soo Sang
    • Journal of Gastric Cancer
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    • v.3 no.1
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    • pp.19-25
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    • 2003
  • Purpose: Dysregulation of apoptosis may attribute to development of cancer by abnormally prolonging cell viability with accumulation of transforming mutations. Survivin and HIAP (Human Inhibitors of Apoptosis)-1 were recently described as apoptosis inhibitors. Their pathogenic roles in gastric cancer are largely unknown. In the present study, we examined the expression of survivin and HIAP-1 in gastric cancer tissues and cell lines in order to elucidate the roles of survivin and HIAP-1 in the process of gastric carcinogenesis. Materials and Methods: Eight gastric cancer cell lines and five gastric cancer tissues were studied. The expression of survivin and HIAP-1 were evaluated by reverse transcription -polymerase chain reaction (RT-PCR), immunohistochemistry, and Western blot. Results: Western blot and RT-PCR analysis revealed survivin and HIAP-1 expression in all gastric cancer cell lines. Increased expression of survivin and HIAP-1 were found in all cases of gastric cancer tissues compared to normal tissues by Western blot analysis. In immunohistochemical analysis tumor cells were stained with anti-survivin and anti-HIAP-1 antibodies. Cell cycle dependence of survivin expression was preserved in gastric cancer cell lines. Conclusion: The results indicate that increased expression of survivin and HIAP-1 genes may play an important role in gastric cancer.

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Expression Analysis of Two Cancer-testis Genes, FBXO39 and TDRD4, in Breast Cancer Tissues and Cell Lines

  • Seifi-Alan, Mahnaz;Shamsi, Roshanak;Ghafouri-Fard, Soudeh;Mirfakhraie, Reza;Zare-Abdollahi, Davood;Movafagh, Abolfazl;Modarressi, Mohammad Hossein;Kazemi, Golnesa;Geranpayeh, Lobat;Najafi-Ashtiani, Mitra
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.11
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    • pp.6625-6629
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    • 2013
  • Breast cancer accounts for one third of new cancer cases among women. The need for biomarkers for early detection is the stimulus to researchers to evaluate altered expression of genes in tumours. Cancer-testis (CT) genes are a group with limited expression in normal tissues except testis but up-regulation in a wide variety of cancers. We here evaluated expression of two CT genes named FBXO39 and TDRD4 in 32 invasive ductal carcinoma samples, 10 fibroadenomas and 6 normal breast tissue samples, in addition to two breast cancer cell lines, MCF-7 and MDA-MB-231, by the means of quantitative real time RT-PCR. FBXO39 showed significant up-regulation in invasive ductal carcinoma samples in comparison with normal samples. It also was expressed in both cell lines and after RHOXF1 gene knock down it was down-regulated in MCF-7 but up-regulated in the MDA-MB-231 cell line. TDRD4 was not expressed in the MCF-7 cell line and any of the tissue samples except testis. However, it was expressed in MDA-MB-231 and was up-regulated after RHOXF1 gene knock down. Our results show that FBXO39 but not TDRD4 can be used for cancer detection and if proved to be immunogenic, might be a putative candidate for breast cancer immunotherapy.

Apoptosis and Cell Cycle Arrest in Two Human Breast Cancer Cell Lines by Dieckol Isolated from Ecklonia cava

  • You, Sun Hyong;Kim, Jeong-Soo;Kim, Yong-Seok
    • Journal of Breast Disease
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    • v.6 no.2
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    • pp.39-45
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    • 2018
  • Purpose: Dieckol, a phlorotannin compound isolated from Ecklonia cava, has been reported to have antioxidant, antiviral, anti-inflammatory, and anticancer properties. The purpose of this study was to investigate its anticancer effects on human breast cancer cell lines. Methods: In this study, the viability of two human breast cancer cell lines SK-BR-3 and MCF-7 was investigated after dieckol treatment using a WST-1 assay. Apoptosis and cell cycle distribution were assayed via Annexin V-fluorescein isothiocyanate and propidium iodide staining followed by flow cytometric analysis. Immunoblotting analysis was also performed using Bax/Bcl-2 to determine whether the dieckol-induced apoptosis was mediated by the intrinsic apoptotic pathway. Results: In a dose dependent manner, dieckol reduced the number of viable cells and increased the number of apoptotic cells. The effect of dieckol on the cell cycle distribution was analyzed using flow cytometry. Dieckol treatment significantly increased the percentage of MCF-7 and SK-BR-3 in the G2/M phase. Immunoblot analysis revealed that 24 hours of dieckol exposure increased the Bax/Bcl-2 ratio. Conclusion: Dieckol induced cytotoxicity in MCF-7 and SK-BR-3 human breast cancer cells inducing apoptosis and cell cycle arrest. Therefore, it is suggested that dieckol may be a potential therapeutic agent for breast cancer.

The Inhibitory Effects of Propolis on In Vitro Proliferation of Human Cancer Cell Lines (Propolis의 인체 암세포 증식억제 효과에 대한 In Vitro 연구)

  • 이현수;이지영;김동청;인만진;황우익
    • Journal of Nutrition and Health
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    • v.33 no.1
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    • pp.80-85
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    • 2000
  • This study was undertaken to investigate the inhibitory effects of propolis on the in vitro proliferation of human colon(HT-29) and hepatoma(HepG2) cancer cell lines. The growth of the HT-29 and HepG2 cells was respectively inhibited by the administration of propolis in a concentration response-dependent manner. The distributions of HT-29 and HepG2 cells cultured in the medium containing propolis were shifted to the smaller sizes, and then HT-29 and HepG2 cells were shrunken under microscopic observations. The progression of cell cycle from G1 to S phase was significantly inhibited by propolis in the HT-29 and HepG2 cell lines, respectively. Those observations suggest that propolis has anticancer effect against some of cancer cell lines in vitro. (Korean J Nutrition 33(1) : 80-85, 2000)

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MiR-130a Overcomes Gefitinib Resistance by Targeting Met in Non-Small Cell Lung Cancer Cell Lines

  • Zhou, Yong-Ming;Liu, Juan;Sun, Wei
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.3
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    • pp.1391-1396
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    • 2014
  • Non-small cell lung cancer (NSCLC) is the most common type of lung cancer and the most common cause of lung cancer death. Currently, the epidermal growth factor receptor inhibitor gefitinib is used for its treatment; however, drug resistance is a major obstacle. Expression of Met has been associated with both primary and acquired resistance to gefitinib, but the mechanisms regulating its expression are not fully understood. Recently, miRNAs such as miR-130a have been shown to play a role in gefitinib resistance, but importance in NSCLC and relationships with Met have not been fully explored. Here we show that miR-130a is over-expressed in gefitinibsensitive NSCLC cell lines, but is low in gefitinib-resistant NSCLC cell lines. Moreover, miR-130a expression was negatively correlated with that of Met. Further analysis revealed that over-expression of miR-130a increased cell apoptosis and inhibited proliferation of NSCLC cells treated with gefitinib, whereas lowering the expression of miR-130a decreased cell apoptosis and promoted cell proliferation after treatment with gefitinib in both gefitinib-sensitive and -resistant NSCLC cell lines, suggesting that miR-130a overcomes gefitinib resistance. We also demonstrated that miR-130a binds to the 3'-UTR of Met and significantly suppresses its expression. Finally, our results showed that over-expressing Met could "rescue" the functions of miR-130a regarding cell apoptosis and proliferation after cells are treated with gefitinib. These findings indicate that the miR-130a/Met axis plays an important role in gefitinib resistance in NSCLC. Thus, the miR-130a/Met axis may be an effective therapeutic target in gefitinib-resistant lung cancer patients.

Portulaca oleracea Seed Oil Exerts Cytotoxic Effects on Human Liver Cancer (HepG2) and Human Lung Cancer (A-549) Cell Lines

  • Al-Sheddi, Ebtesam Saad;Farshori, Nida Nayyar;Al-Oqail, Mai Mohammad;Musarrat, Javed;Al-Khedhairy, Abdulaziz Ali;Siddiqui, Maqsood Ahmed
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.8
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    • pp.3383-3387
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    • 2015
  • Portulaca oleracea (Family: Portulacaceae), is well known for its anti-inflammatory, antioxidative, anti-bacterial, and anti-tumor activities. However, cytotoxic effects of seed oil of Portulaca oleracea against human liver cancer (HepG2) and human lung cancer (A-549) cell lines have not been studied previously. Therefore, the present study was designed to investigate the cytotoxic effects of Portulaca oleracea seed oil on HepG2 and A-549 cell lines. Both cell lines were exposed to various concentrations of Portulaca oleracea seed oil for 24h. After the exposure, percentage cell viability was studied by (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) (MTT), neutral red uptake (NRU) assays, and cellular morphology by phase contrast inverted microscopy. The results showed a concentration-dependent significant reduction in the percentage cell viability and an alteration in the cellular morphology of HepG2 and A-549 cells. The percentage cell viability was recorded as 73%, 63%, and 54% by MTT assay and 76%, 61%, and 50% by NRU assay at 250, 500, and $1000{\mu}g/ml$, respectively in HepG2 cells. Percentage cell viability was recorded as 82%, 72%, and 64% by MTT assay and 83%, 68%, and 56% by NRU assay at 250, 500, and $1000{\mu}g/ml$, respectively in A-549 cells. The 100 $100{\mu}g/ml$ and lower concentrations were found to be non cytotoxic to A-549 cells, whereas decrease of 14% and 12% were recorded by MTT and NRU assay, respectively in HepG2 cells. Both HepG2 and A-549 cell lines exposed to 250, 500, and $1000{\mu}g/ml$ of Portulaca oleracea seed oil lost their normal morphology, cell adhesion capacity, become rounded, and appeared smaller in size. The data from this study showed that exposure to seed oil of Portulaca oleracea resulted in significant cytotoxicity and inhibition of growth of the human liver cancer (HepG2) and human lung cancer (A-549) cell lines.

Long Non-coding RNAs are Differentially Expressed in Hepatocellular Carcinoma Cell Lines with Differing Metastatic Potential

  • Fang, Ting-Ting;Sun, Xiao-Jing;Chen, Jie;Zhao, Yan;Sun, Rui-Xia;Ren, Ning;Liu, Bin-Bin
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.23
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    • pp.10513-10524
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    • 2015
  • Background: Metastasis is a major reason for poor prognosis in patients with cancer, including hepatocellular carcinoma (HCC). A salient feature is the ability of cancer cells to colonize different organs. Long non-coding RNAs (lncRNAs) play important roles in numerous cellular processes, including metastasis. Materials and Methods: In this study, the lncRNA expression profiles of two HCC cell lines, one with high potential for metastasis to the lung (HCCLM3) and the other to lymph nodes (HCCLYM-H2) were assessed using the Arraystar Human LncRNA Array v2.0, which contains 33,045 lncRNAs and 30,215 mRNAs. Coding-non-coding gene co-expression (CNC) networks were constructed and gene set enrichment analysis (GSEA) was performed to identify lncRNAs with potential functions in organ-specific metastasis. Levels of two representative lncRNAs and one representative mRNA, RP5-1014O16.1, lincRNA-TSPAN8 and TSPAN8, were further detected in HCC cell lines with differing metastasis potential by qRT-PCR. Results: Using microarray data, we identified 1,482 lncRNAs and 1,629 mRNAs that were differentially expressed (${\geq}1.5$ fold-change) between the two HCC cell lines. The most upregulated lncRNAs in H2 were RP11-672F9.1, RP5-1014O16.1, and RP11-501G6.1, while the most downregulated ones were lincRNA-TSPAN8, lincRNA-CALCA, C14orf132, NCRNA00173, and CR613944. The most upregulated mRNAs in H2 were C15orf48, PSG2, and PSG8, while the most downregulated ones were CALCB, CD81, CD24, TSPAN8, and SOST. Among them, lincRNA-TSPAN8 and TSPAN8 were found highly expressed in high lung metastatic potential HCC cells, while lowly expressed in no or low lung metastatic potential HCC cells. RP5-1014O16.1 was highly expressed in high lymphatic metastatic potential HCC cell lines, while lowly expressed in no lymphatic metastatic potential HCC cell lines. Conclusions: We provide the first detailed description of lncRNA expression profiles related to organ-specific metastasis in HCC. We demonstrated that a large number of lncRNAs may play important roles in driving HCC cells to metastasize to different sites; these lncRNAs may provide novel molecular biomarkers and offer a new basis for combating metastasis in HCC cases.

Establishment of Highly Tumorigenic Human Gastric Carcinoma Cell Lines from Xenograft Tumors in Mice

  • Song, Kyung-A;Park, Jihyun;Kim, Ha-Jung;Kang, Myung Soo;Kim, Sun Young
    • Biomedical Science Letters
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    • v.23 no.3
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    • pp.238-250
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    • 2017
  • Patient's primary tumor-derived tumor cell lines likely represent ideal tools for human tumor biology in vitro and in vivo. Here, we describe eight human gastric carcinoma cell lines derived from established tumors in vivo upon subcutaneous transplantation of primary gastric carcinoma specimens in BALB/c nude mice. These xenografted gastric tumor cell lines (GTX) displayed close similarity with primary gastric tumor tissues in their in vivo growth pattern and genomic alterations. GTX-085 cells were resistant to cisplatin, while GTX-087 was the most sensitive cell line. GTX-085 was the only cell line showing a metastatic potential. Epithelial cell adhesion molecule (EPCAM) expression was especially strong in all tissue samples, as well as in cell cultures. GTX-139, the largest tumor graft obtained after injection, displayed distinct expression of CD44v6, fibroblast growth factor receptor 2 (FGFR2), and prominin 1 (PROM1, also known as CD133). In summary, we established eight xenograft gastric cancer cell lines from gastric cancer patient tissues, with their histological and molecular features consistent with those of the primary tumors. The established GTX cell lines will enable future studies of their responses to various treatments for gastric cancer.

Effects of Non-Cytotoxic Concentration of Anticancer Drugs on Doxorubicin Cytotoxicity in Human Breast Cancer Cell Lines

  • Lee, Yoon-Ik;Lee, Young-Ik
    • BMB Reports
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    • v.29 no.4
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    • pp.314-320
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    • 1996
  • The effects of non-cytotoxic concentrations of tamoxifen, verapamil, and trifluoperazine on doxorubicin cytotoxicity in five human breast cancer cell lines were studied. A non-cytotoxic concentration of tamoxifen resulted in enhanced doxorubicin cytotoxicity in HTB-123, HTB-26, and MCF-7. In these three cell lines, a combination of tamoxifen with verapamil resulted in even more increased doxorubicin cytotoxicity. Addition of verapamil or trifluoperazine alone did not influence the doxorubicin cytotoxicity significantly. Only in HTB-19 did coincubation with verapamil increase the doxorubicin cytotoxicity. In HTB-123, combination of tamoxifen with trifluoperazine increased the doxorubicin cytotoxicity significantly. In the cell lines where co-incubation with tamoxifen increased doxorubicin sensitivity, high estrogen receptor expression was detected. However, HTB-20, where tamoxifen did not enhance doxorubicin action, was also estrogen receptor positive. None of the cell lines had multidrug resistance related drug efflux and drug retention was not increased by the treatment with tamoxifen and verapamil. Cell cycle traverses were not altered by incubation with tamoxifen, verapamil or combinations thereof. These observatlons suggest mechanism of non-cytotoxic concentrations of tamoxifen and verapamil on doxorubicin cytotoxicity may involve one or more other cellular processes besides those of interference of estrogen binding to its receptor, cell cycle perturbation, or drug efflux blocking.

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In Vitro Cytotoxic Activity of Seed Oil of Fenugreek Against Various Cancer Cell Lines

  • Al-Oqail, Mai Mohammad;Farshori, Nida Nayyar;Al-Sheddi, Ebtesam Saad;Musarrat, Javed;Al-Khedhairy, Abdulaziz Ali;Siddiqui, Maqsood Ahmed
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.3
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    • pp.1829-1832
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    • 2013
  • In the present study, investigations were carried out to screen the anticancer activities of fenugreek seed oil against cancer cell lines (HEp-2, MCF-7, WISH cells), and a normal cell line (Vero cells). Cytotoxicity was assessed with MTT and NRU assays, and cellular morphological alterations were studied using phase contrast light microscopy. All cells were exposed toi 10-1000 ${\mu}g/ml$ of fenugreek seed oil for 24 h. The results show that fenugreek seed oil significantly reduced the cell viability, and altered the cellular morphology in a dose dependent manner. Among the cell lines, HEp-2 cells showed the highest decrease in cell viability, followed by MCF-7, WISH, and Vero cells by MTT and NRU assays. Cell viability at 1000 ${\mu}g/ml$ was recorded as 55% in HEp-2 cells, 67% in MCF-7 cells, 75% in WISH cells, and 86% in Vero cells. The present study provides preliminary screening data for fenugreek seed oil pointing to potent cytotoxicity against cancer cells.